TY  - CONF
AU  - Anđus, Pavle
AU  - Perić, Mina
AU  - Nikolić, Ljiljana
AU  - Bataveljić, Danijela
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5513
AB  - Non-neuronal cells of glial origin play an essential
role in ALS onset and progression. Amer gaining
knowledge on the role of astrocytes in the disease
with particular reference to the inwardly rectifying
potassium channel Kir4.1 we aimed to examine the
functional properties of microglia and oligodendrocytes in the spinal cord of the ALS SOD1G93A rat
focusing on the expression and functional signilcance of Kir4.1.
Microglia in the ALS rat spinal cords showed
remarkable clustering in ventral horns, already in
presymptomatic animals. Colocalization of Kir4.1
and microglial Iba1 staining was 2-3 times more
abundant in presymptomatic as well as in symptomatic animals compared to individual cells. It was
also shown that these clusters bare a higher accumulation and colocalization of Kir4.1 and Iba1 with
mutated SOD1 compared to individual cells.
se spinal cord microglial cells were cultured and
patch-clamped using an innovative movable microscope stage to facilitate the gigaseal formation.
sese measurements demonstrated a decrease of
Ba2+-sensitive Kir currents.
se expression of Kir4.1 was markedly diminished in the dysmorphic ALS oligodendrocytes of
the degenerative phenotype. se cells isolated and
cultured from the SOD1G93A spinal cord showed
no change in processes ramilcation, but expressed
a lower level of Kir4.1. Whole-cell patch-clamp
recordings revealed compromised membrane
biophysical properties and diminished inward currents in ALS oligodendrocytes, with a particularly
decreased Ba2+-sensitive Kir current.
Altogether, our lndings provide the evidence
of a modiled Kir4.1 expression and function in
SOD1G93A glia with this channel’s particular abundance in clusters resembling ALS-specilc plaques.
PB  - Zagreb: Department of Neurology, University Hospital Centre Zagreb
C3  - Abstracts: International Conference on Neurological Disorders and Neurorestoration; 2022 May 19-22; Dubrovnik, Croatia
T1  - Kir4.1 channel- A universal target in ALS glia
SP  - 13
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5513
ER  - 

@conference{
editor = "Mitrečić, Dinko, Petravić, Damir",
author = "Anđus, Pavle and Perić, Mina and Nikolić, Ljiljana and Bataveljić, Danijela",
year = "2022",
abstract = "Non-neuronal cells of glial origin play an essential
role in ALS onset and progression. Amer gaining
knowledge on the role of astrocytes in the disease
with particular reference to the inwardly rectifying
potassium channel Kir4.1 we aimed to examine the
functional properties of microglia and oligodendrocytes in the spinal cord of the ALS SOD1G93A rat
focusing on the expression and functional signilcance of Kir4.1.
Microglia in the ALS rat spinal cords showed
remarkable clustering in ventral horns, already in
presymptomatic animals. Colocalization of Kir4.1
and microglial Iba1 staining was 2-3 times more
abundant in presymptomatic as well as in symptomatic animals compared to individual cells. It was
also shown that these clusters bare a higher accumulation and colocalization of Kir4.1 and Iba1 with
mutated SOD1 compared to individual cells.
se spinal cord microglial cells were cultured and
patch-clamped using an innovative movable microscope stage to facilitate the gigaseal formation.
sese measurements demonstrated a decrease of
Ba2+-sensitive Kir currents.
se expression of Kir4.1 was markedly diminished in the dysmorphic ALS oligodendrocytes of
the degenerative phenotype. se cells isolated and
cultured from the SOD1G93A spinal cord showed
no change in processes ramilcation, but expressed
a lower level of Kir4.1. Whole-cell patch-clamp
recordings revealed compromised membrane
biophysical properties and diminished inward currents in ALS oligodendrocytes, with a particularly
decreased Ba2+-sensitive Kir current.
Altogether, our lndings provide the evidence
of a modiled Kir4.1 expression and function in
SOD1G93A glia with this channel’s particular abundance in clusters resembling ALS-specilc plaques.",
publisher = "Zagreb: Department of Neurology, University Hospital Centre Zagreb",
journal = "Abstracts: International Conference on Neurological Disorders and Neurorestoration; 2022 May 19-22; Dubrovnik, Croatia",
title = "Kir4.1 channel- A universal target in ALS glia",
pages = "13",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5513"
}

Mitrečić, D., Petravić, D., Anđus, P., Perić, M., Nikolić, L.,& Bataveljić, D.. (2022). Kir4.1 channel- A universal target in ALS glia. in Abstracts: International Conference on Neurological Disorders and Neurorestoration; 2022 May 19-22; Dubrovnik, Croatia
Zagreb: Department of Neurology, University Hospital Centre Zagreb., 13.
https://hdl.handle.net/21.15107/rcub_ibiss_5513

Mitrečić D, Petravić D, Anđus P, Perić M, Nikolić L, Bataveljić D. Kir4.1 channel- A universal target in ALS glia. in Abstracts: International Conference on Neurological Disorders and Neurorestoration; 2022 May 19-22; Dubrovnik, Croatia. 2022;:13.
https://hdl.handle.net/21.15107/rcub_ibiss_5513 .

Mitrečić, Dinko, Petravić, Damir, Anđus, Pavle, Perić, Mina, Nikolić, Ljiljana, Bataveljić, Danijela, "Kir4.1 channel- A universal target in ALS glia" in Abstracts: International Conference on Neurological Disorders and Neurorestoration; 2022 May 19-22; Dubrovnik, Croatia (2022):13,
https://hdl.handle.net/21.15107/rcub_ibiss_5513 .

TY  - JOUR
AU  - Mandić, Marija
AU  - Mitić, Katarina
AU  - Nedeljković, Predrag
AU  - Perić, Mina
AU  - Božić, Bojan
AU  - Lunić, Tanja
AU  - Bačić, Ana
AU  - Rajilić-Stojanović, Mirjana
AU  - Peković, Sanja
AU  - Božić Nedeljković, Biljana
PY  - 2022
UR  - https://www.mdpi.com/2072-6643/14/6/1273
UR  - http://www.ncbi.nlm.nih.gov/pubmed/35334928
UR  - http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=PMC8955508
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4940
AB  - The present study aimed to investigate the neuroprotective effects of the vitamin B complex (B1, B2, B3, B5, B6, and B12-VBC), by studying the changes in the femoral nerve, quadriceps muscle, popliteal lymph nodes and gut microbiota in the rat model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). VBC treatment attenuated clinical signs of EAE during the disease, and reduced the duration of EAE thereby contributing to a faster recovery. In VBC-treated EAE rats, a significant decrease in nerve and muscle nuclear density was revealed during the onset period of the disease, while a marked increase was detected at the end of the disease, compared with untreated EAE rats. In the lymph nodes of VBC-treated EAE rats, a fewer number of lymphoid follicles in the cortical area and smaller epithelioid granulomas were detected. The changes in microbiota composition were examined using 16S rRNA gene sequencing and bioinformatics analysis, which revealed the potential of VBC treatment in establishing and/or maintaining gut microbiota homeostasis. Finally, the present study demonstrated that VBC treatment ameliorated the cellular changes in the affected peripheral nerve, muscles innervated by this nerve, and the gut microbiota dysbiosis which occurred during the EAE.
PB  - Basel: MDPI
T2  - Nutrients
T1  - Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis.
IS  - 6
VL  - 14
DO  - 10.3390/nu14061273
SP  - 1273
ER  - 

@article{
author = "Mandić, Marija and Mitić, Katarina and Nedeljković, Predrag and Perić, Mina and Božić, Bojan and Lunić, Tanja and Bačić, Ana and Rajilić-Stojanović, Mirjana and Peković, Sanja and Božić Nedeljković, Biljana",
year = "2022",
abstract = "The present study aimed to investigate the neuroprotective effects of the vitamin B complex (B1, B2, B3, B5, B6, and B12-VBC), by studying the changes in the femoral nerve, quadriceps muscle, popliteal lymph nodes and gut microbiota in the rat model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). VBC treatment attenuated clinical signs of EAE during the disease, and reduced the duration of EAE thereby contributing to a faster recovery. In VBC-treated EAE rats, a significant decrease in nerve and muscle nuclear density was revealed during the onset period of the disease, while a marked increase was detected at the end of the disease, compared with untreated EAE rats. In the lymph nodes of VBC-treated EAE rats, a fewer number of lymphoid follicles in the cortical area and smaller epithelioid granulomas were detected. The changes in microbiota composition were examined using 16S rRNA gene sequencing and bioinformatics analysis, which revealed the potential of VBC treatment in establishing and/or maintaining gut microbiota homeostasis. Finally, the present study demonstrated that VBC treatment ameliorated the cellular changes in the affected peripheral nerve, muscles innervated by this nerve, and the gut microbiota dysbiosis which occurred during the EAE.",
publisher = "Basel: MDPI",
journal = "Nutrients",
title = "Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis.",
number = "6",
volume = "14",
doi = "10.3390/nu14061273",
pages = "1273"
}

Mandić, M., Mitić, K., Nedeljković, P., Perić, M., Božić, B., Lunić, T., Bačić, A., Rajilić-Stojanović, M., Peković, S.,& Božić Nedeljković, B.. (2022). Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis.. in Nutrients
Basel: MDPI., 14(6), 1273.
https://doi.org/10.3390/nu14061273

Mandić M, Mitić K, Nedeljković P, Perić M, Božić B, Lunić T, Bačić A, Rajilić-Stojanović M, Peković S, Božić Nedeljković B. Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis.. in Nutrients. 2022;14(6):1273.
doi:10.3390/nu14061273 .

Mandić, Marija, Mitić, Katarina, Nedeljković, Predrag, Perić, Mina, Božić, Bojan, Lunić, Tanja, Bačić, Ana, Rajilić-Stojanović, Mirjana, Peković, Sanja, Božić Nedeljković, Biljana, "Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis." in Nutrients, 14, no. 6 (2022):1273,
https://doi.org/10.3390/nu14061273 . .

TY  - JOUR
AU  - Perić, Mina
AU  - Bataveljić, Danijela
AU  - Bijelić, Dunja
AU  - Milićević, Katarina
AU  - Andjus, Pavle R.
AU  - Bogdanović Pristov, Jelena
AU  - Nikolić, Ljiljana
PY  - 2022
UR  - https://onlinelibrary.wiley.com/doi/10.1002/jemt.24066
UR  - http://www.ncbi.nlm.nih.gov/pubmed/35088507
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/4790
AB  - We describe an approach for studying the physiology of single live cells using the conceptionally novel upright microscope/patch-clamp configuration. Electrophysiology experiments typically require a microscope with the fixed stage position and the motion control of the microscope objective. Here, we demonstrate that a microscope with a z-axis movable stage and a fixed objective can also be efficiently used in combination with the patch-clamp technique. We define a set of underlying principles governing the operation of this microscope/patch-clamp configuration and demonstrate its performance in practice using cultured astrocytes, microglia, and oligodendrocytes. Experimental results show that our custom configuration provides stable recordings, has a high success rate of the whole-cell patch-clamp trials, can be effectively applied to study cellular physiology of glial cells, and provides comparable performance and usability to the commercially available systems. Our system can be easily replicated or adapted to suit the needs of the research groups and can be cost-effective in reducing the investments in purchasing additional equipment. We provide step-by-step instructions on implementing an upright microscope with z-axis movable stage as a routine workhorse for patch-clamping.
PB  - Hoboken: John Wiley and Sons Inc.
T2  - Microscopy Research and Technique
T1  - Approach for patch-clamping using an upright microscope with z-axis movable stage.
IS  - 6
VL  - 85
DO  - 10.1002/jemt.24066
SP  - 2095
EP  - 2104
ER  - 

@article{
author = "Perić, Mina and Bataveljić, Danijela and Bijelić, Dunja and Milićević, Katarina and Andjus, Pavle R. and Bogdanović Pristov, Jelena and Nikolić, Ljiljana",
year = "2022",
abstract = "We describe an approach for studying the physiology of single live cells using the conceptionally novel upright microscope/patch-clamp configuration. Electrophysiology experiments typically require a microscope with the fixed stage position and the motion control of the microscope objective. Here, we demonstrate that a microscope with a z-axis movable stage and a fixed objective can also be efficiently used in combination with the patch-clamp technique. We define a set of underlying principles governing the operation of this microscope/patch-clamp configuration and demonstrate its performance in practice using cultured astrocytes, microglia, and oligodendrocytes. Experimental results show that our custom configuration provides stable recordings, has a high success rate of the whole-cell patch-clamp trials, can be effectively applied to study cellular physiology of glial cells, and provides comparable performance and usability to the commercially available systems. Our system can be easily replicated or adapted to suit the needs of the research groups and can be cost-effective in reducing the investments in purchasing additional equipment. We provide step-by-step instructions on implementing an upright microscope with z-axis movable stage as a routine workhorse for patch-clamping.",
publisher = "Hoboken: John Wiley and Sons Inc.",
journal = "Microscopy Research and Technique",
title = "Approach for patch-clamping using an upright microscope with z-axis movable stage.",
number = "6",
volume = "85",
doi = "10.1002/jemt.24066",
pages = "2095-2104"
}

Perić, M., Bataveljić, D., Bijelić, D., Milićević, K., Andjus, P. R., Bogdanović Pristov, J.,& Nikolić, L.. (2022). Approach for patch-clamping using an upright microscope with z-axis movable stage.. in Microscopy Research and Technique
Hoboken: John Wiley and Sons Inc.., 85(6), 2095-2104.
https://doi.org/10.1002/jemt.24066

Perić M, Bataveljić D, Bijelić D, Milićević K, Andjus PR, Bogdanović Pristov J, Nikolić L. Approach for patch-clamping using an upright microscope with z-axis movable stage.. in Microscopy Research and Technique. 2022;85(6):2095-2104.
doi:10.1002/jemt.24066 .

Perić, Mina, Bataveljić, Danijela, Bijelić, Dunja, Milićević, Katarina, Andjus, Pavle R., Bogdanović Pristov, Jelena, Nikolić, Ljiljana, "Approach for patch-clamping using an upright microscope with z-axis movable stage." in Microscopy Research and Technique, 85, no. 6 (2022):2095-2104,
https://doi.org/10.1002/jemt.24066 . .

TY  - CONF
AU  - Perić, Mina
AU  - Nikolić, Ljiljana
AU  - Bataveljić, Danijela
AU  - Andjus, Pavle
PY  - 2022
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5511
AB  - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by death of motor neurons in the spinal cord and brain. Non-neuronal cells particularly of glial origin play an essential role in disease onset and progression. The aim of our study was to examine functional properties of two glial species of the spinal cord, oligodendrocytes and microglia in the ALS SOD1G93A rat with a particular focus on the expression and functional significance of the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells. 
We demonstrate that the expression of Kir4.1 is markedly diminished in oligodendrocytes of the SOD1G93A rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes, indicative of a degenerative phenotype. To assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. The cells isolated from the SOD1G93A spinal cord displayed similar processes ramification as the control, but expressed a lower level of Kir4.1. Whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in ALS oligodendrocytes, while the Ba2+-sensitive Kir current was decreased in ALS oligodendrocytes [1]. 
The microglia in the ALS rat spinal chords shows remarkable clustering in ventral horns, already starting in presymptomatic animals. Colocalization of Kir4.1 and microglial Iba1 staining was 2-3 times more abudant in presymptomatic as well as in symptomatic animals compared to individual cells. The morphology of micorglia also changes in ALS where the number and length of processes dicreases almost the same in pre- and symptomatic animals. It was also shown that these clusters bare a higher accumulation and colocalization with Kir4.1 and Iba1 of mutated SOD1 compared to individual cells. Similarly, the transmembrane marker of microglial fagocitosis, CD68 was also augmented in these clusters. 
The spinal chord micorglial cells were cultured and explored with patch-clamp electrophysiology by using an innovative movable microscope stage [2] to facilitate the gigaseal formation of the cell membrane and patch pipette. These measurements demonstrated a decrease of Kir Ba2+-sensitive currents.
Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in SOD1G93A spinal cord oligodendrocytes and microglia with this channel’s particular abundance in clusters typical of ALS pathology and its progression.
REFERENCES
[1]	M.Peric, L. Nikolic L, et al. Eur J Neurosci. 54 (2021), 6339-6354.
[2]	M.Peric, D. Bataveljić et al. Microsc Res Tech. (2022) , DOI: 10.1002/jemt.24066
PB  - Belgrade: Institute of Physics
C3  - Book of Abstracts: 15th Photonics Workshop: Conference; 2022 Mar 13-16; Kopaonik, Serbia
T1  - Imaging the molecular markers of neurodegeneration in the ALS rat oligodendrocytes and microglia
SP  - 35
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5511
ER  - 

@conference{
author = "Perić, Mina and Nikolić, Ljiljana and Bataveljić, Danijela and Andjus, Pavle",
year = "2022",
abstract = "Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by death of motor neurons in the spinal cord and brain. Non-neuronal cells particularly of glial origin play an essential role in disease onset and progression. The aim of our study was to examine functional properties of two glial species of the spinal cord, oligodendrocytes and microglia in the ALS SOD1G93A rat with a particular focus on the expression and functional significance of the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells. 
We demonstrate that the expression of Kir4.1 is markedly diminished in oligodendrocytes of the SOD1G93A rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes, indicative of a degenerative phenotype. To assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. The cells isolated from the SOD1G93A spinal cord displayed similar processes ramification as the control, but expressed a lower level of Kir4.1. Whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in ALS oligodendrocytes, while the Ba2+-sensitive Kir current was decreased in ALS oligodendrocytes [1]. 
The microglia in the ALS rat spinal chords shows remarkable clustering in ventral horns, already starting in presymptomatic animals. Colocalization of Kir4.1 and microglial Iba1 staining was 2-3 times more abudant in presymptomatic as well as in symptomatic animals compared to individual cells. The morphology of micorglia also changes in ALS where the number and length of processes dicreases almost the same in pre- and symptomatic animals. It was also shown that these clusters bare a higher accumulation and colocalization with Kir4.1 and Iba1 of mutated SOD1 compared to individual cells. Similarly, the transmembrane marker of microglial fagocitosis, CD68 was also augmented in these clusters. 
The spinal chord micorglial cells were cultured and explored with patch-clamp electrophysiology by using an innovative movable microscope stage [2] to facilitate the gigaseal formation of the cell membrane and patch pipette. These measurements demonstrated a decrease of Kir Ba2+-sensitive currents.
Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in SOD1G93A spinal cord oligodendrocytes and microglia with this channel’s particular abundance in clusters typical of ALS pathology and its progression.
REFERENCES
[1]	M.Peric, L. Nikolic L, et al. Eur J Neurosci. 54 (2021), 6339-6354.
[2]	M.Peric, D. Bataveljić et al. Microsc Res Tech. (2022) , DOI: 10.1002/jemt.24066",
publisher = "Belgrade: Institute of Physics",
journal = "Book of Abstracts: 15th Photonics Workshop: Conference; 2022 Mar 13-16; Kopaonik, Serbia",
title = "Imaging the molecular markers of neurodegeneration in the ALS rat oligodendrocytes and microglia",
pages = "35",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5511"
}

Perić, M., Nikolić, L., Bataveljić, D.,& Andjus, P.. (2022). Imaging the molecular markers of neurodegeneration in the ALS rat oligodendrocytes and microglia. in Book of Abstracts: 15th Photonics Workshop: Conference; 2022 Mar 13-16; Kopaonik, Serbia
Belgrade: Institute of Physics., 35.
https://hdl.handle.net/21.15107/rcub_ibiss_5511

Perić M, Nikolić L, Bataveljić D, Andjus P. Imaging the molecular markers of neurodegeneration in the ALS rat oligodendrocytes and microglia. in Book of Abstracts: 15th Photonics Workshop: Conference; 2022 Mar 13-16; Kopaonik, Serbia. 2022;:35.
https://hdl.handle.net/21.15107/rcub_ibiss_5511 .

Perić, Mina, Nikolić, Ljiljana, Bataveljić, Danijela, Andjus, Pavle, "Imaging the molecular markers of neurodegeneration in the ALS rat oligodendrocytes and microglia" in Book of Abstracts: 15th Photonics Workshop: Conference; 2022 Mar 13-16; Kopaonik, Serbia (2022):35,
https://hdl.handle.net/21.15107/rcub_ibiss_5511 .

TY  - JOUR
AU  - Perić, Mina
AU  - Nikolić, Ljiljana
AU  - Anđus, Pavle R.
AU  - Bataveljić, Danijela
PY  - 2021
UR  - https://onlinelibrary.wiley.com/doi/10.1111/ejn.15451
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4486
AB  - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Although this disease is characterized by motoneuron degeneration, non-neuronal cells such as oligodendrocytes play an important role in the disease onset and progression. The aim of our study was to examine functional properties of oligodendrocytes in the SOD1G93A rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells and plays a role in the regulation of extracellular K+ . First, we demonstrate that the expression of Kir4.1 is diminished in the spinal cord oligodendrocytes of the SOD1G93A rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes in the ALS spinal cord that is indicative of a degenerative phenotype. In order to assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. Oligodendrocytes isolated from the SOD1G93A spinal cord display similar ramification of the processes as the control but express a lower level of Kir4.1. We further demonstrate an impairment of oligodendrocyte functional properties in ALS. Remarkably, whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in the SOD1G93A oligodendrocytes. In addition, the Ba2+ -sensitive Kir currents were decreased in ALS oligodendrocytes. Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in oligodendrocytes of the SOD1G93A spinal cord, suggesting oligodendrocyte Kir4.1 channel as a potential contributor to the ALS pathophysiology.
PB  - Hoboken: John Wiley and Sons Inc.
T2  - European Journal of Neuroscience
T1  - Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.
IS  - 7
VL  - 54
DO  - 10.1111/ejn.15451
SP  - 6339
EP  - 6354
ER  - 

@article{
author = "Perić, Mina and Nikolić, Ljiljana and Anđus, Pavle R. and Bataveljić, Danijela",
year = "2021",
abstract = "Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Although this disease is characterized by motoneuron degeneration, non-neuronal cells such as oligodendrocytes play an important role in the disease onset and progression. The aim of our study was to examine functional properties of oligodendrocytes in the SOD1G93A rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells and plays a role in the regulation of extracellular K+ . First, we demonstrate that the expression of Kir4.1 is diminished in the spinal cord oligodendrocytes of the SOD1G93A rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes in the ALS spinal cord that is indicative of a degenerative phenotype. In order to assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. Oligodendrocytes isolated from the SOD1G93A spinal cord display similar ramification of the processes as the control but express a lower level of Kir4.1. We further demonstrate an impairment of oligodendrocyte functional properties in ALS. Remarkably, whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in the SOD1G93A oligodendrocytes. In addition, the Ba2+ -sensitive Kir currents were decreased in ALS oligodendrocytes. Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in oligodendrocytes of the SOD1G93A spinal cord, suggesting oligodendrocyte Kir4.1 channel as a potential contributor to the ALS pathophysiology.",
publisher = "Hoboken: John Wiley and Sons Inc.",
journal = "European Journal of Neuroscience",
title = "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.",
number = "7",
volume = "54",
doi = "10.1111/ejn.15451",
pages = "6339-6354"
}

Perić, M., Nikolić, L., Anđus, P. R.,& Bataveljić, D.. (2021). Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.. in European Journal of Neuroscience
Hoboken: John Wiley and Sons Inc.., 54(7), 6339-6354.
https://doi.org/10.1111/ejn.15451

Perić M, Nikolić L, Anđus PR, Bataveljić D. Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis.. in European Journal of Neuroscience. 2021;54(7):6339-6354.
doi:10.1111/ejn.15451 .

Perić, Mina, Nikolić, Ljiljana, Anđus, Pavle R., Bataveljić, Danijela, "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis." in European Journal of Neuroscience, 54, no. 7 (2021):6339-6354,
https://doi.org/10.1111/ejn.15451 . .

TY  - CONF
AU  - Perić, Mina
AU  - Nikolić, Ljiljana
AU  - Anđus, Pavle R.
AU  - Bataveljić, Danijela
PY  - 2020
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5499
AB  - Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting lower
and upper motor neurons, leading to muscle atrophy, paralysis and death. Although
ALS is characterized by motoneuron degeneration, non-neuronal cells such as
oligodendrocytes play an essential role in disease onset and progression. The aim
of this study was to investigate functional properties of oligodendrocytes in the ALS
with particular focus on their role in the regulation of extracellular K+ through inwardly
rectifying potassium channel Kir4.1 abundantly expressed in these glial cells. We
employed immunolabeling of Kir4.1, and oligodendrocyte-specific marker CNPase,
to examine the expression of Kir4.1 in oligodendrocytes of the lumbar spinal cord of
SOD1G93A rat model of ALS. Furthermore, whole-cell patch-clamp recordings were
performed on primary oligodendrocyte cultures from ALS and control rats to
investigate functional properties of these cells. Our data show reduced expression
of Kir4.1 in the oligodendrocytes in the lumbar spinal cord of SOD1G93A rat compared
to control. Moreover, we found elevated number of dysmorphic oligodendrocytes in
the ALS spinal cord, indicative of a degenerative phenotype. Oligodendrocytes
isolated from SOD1G93A spinal cord display similar processes ramification as the
control, however expressing a lower level of Kir4.1. Electrophysiological examination
of cultured SOD1G93A oligodendrocytes revealed compromised membrane
properties and diminished inward currents in comparison to control. In addition, the
Ba2+-sensitive Kir current is decreased in ALS oligodendrocytes. Altogether, our
findings provide the evidence of impaired Kir4.1 expression and function in
SOD1G93A spinal cord oligodendrocytes suggesting a critical role of oligodendrocyte
Kir4.1 channel in ALS pathophysiology.
PB  - Querétaro, México: Instituto de neurobiologia
C3  - Proceedings: 3rd Symposium on Physiology and pathology of neuroglia; 2020 Noc 24-25; Virtual
T1  - Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis
SP  - 75
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5499
ER  - 

@conference{
author = "Perić, Mina and Nikolić, Ljiljana and Anđus, Pavle R. and Bataveljić, Danijela",
year = "2020",
abstract = "Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease affecting lower
and upper motor neurons, leading to muscle atrophy, paralysis and death. Although
ALS is characterized by motoneuron degeneration, non-neuronal cells such as
oligodendrocytes play an essential role in disease onset and progression. The aim
of this study was to investigate functional properties of oligodendrocytes in the ALS
with particular focus on their role in the regulation of extracellular K+ through inwardly
rectifying potassium channel Kir4.1 abundantly expressed in these glial cells. We
employed immunolabeling of Kir4.1, and oligodendrocyte-specific marker CNPase,
to examine the expression of Kir4.1 in oligodendrocytes of the lumbar spinal cord of
SOD1G93A rat model of ALS. Furthermore, whole-cell patch-clamp recordings were
performed on primary oligodendrocyte cultures from ALS and control rats to
investigate functional properties of these cells. Our data show reduced expression
of Kir4.1 in the oligodendrocytes in the lumbar spinal cord of SOD1G93A rat compared
to control. Moreover, we found elevated number of dysmorphic oligodendrocytes in
the ALS spinal cord, indicative of a degenerative phenotype. Oligodendrocytes
isolated from SOD1G93A spinal cord display similar processes ramification as the
control, however expressing a lower level of Kir4.1. Electrophysiological examination
of cultured SOD1G93A oligodendrocytes revealed compromised membrane
properties and diminished inward currents in comparison to control. In addition, the
Ba2+-sensitive Kir current is decreased in ALS oligodendrocytes. Altogether, our
findings provide the evidence of impaired Kir4.1 expression and function in
SOD1G93A spinal cord oligodendrocytes suggesting a critical role of oligodendrocyte
Kir4.1 channel in ALS pathophysiology.",
publisher = "Querétaro, México: Instituto de neurobiologia",
journal = "Proceedings: 3rd Symposium on Physiology and pathology of neuroglia; 2020 Noc 24-25; Virtual",
title = "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis",
pages = "75",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5499"
}

Perić, M., Nikolić, L., Anđus, P. R.,& Bataveljić, D.. (2020). Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis. in Proceedings: 3rd Symposium on Physiology and pathology of neuroglia; 2020 Noc 24-25; Virtual
Querétaro, México: Instituto de neurobiologia., 75.
https://hdl.handle.net/21.15107/rcub_ibiss_5499

Perić M, Nikolić L, Anđus PR, Bataveljić D. Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis. in Proceedings: 3rd Symposium on Physiology and pathology of neuroglia; 2020 Noc 24-25; Virtual. 2020;:75.
https://hdl.handle.net/21.15107/rcub_ibiss_5499 .

Perić, Mina, Nikolić, Ljiljana, Anđus, Pavle R., Bataveljić, Danijela, "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis" in Proceedings: 3rd Symposium on Physiology and pathology of neuroglia; 2020 Noc 24-25; Virtual (2020):75,
https://hdl.handle.net/21.15107/rcub_ibiss_5499 .

TY  - JOUR
AU  - Dakić, Tamara B.
AU  - Jevđović, Tanja V.
AU  - Perić, Mina I.
AU  - Bjelobaba, Ivana
AU  - Markelić, Milica B.
AU  - Milutinović, Bojana S.
AU  - Lakić, Iva V.
AU  - Jasnić, Nebojša I.
AU  - Đorđević, Jelena D.
AU  - Vujović, Predrag Z.
PY  - 2017
UR  - http://doi.wiley.com/10.1111/ejn.13607
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/2779
AB  - In the hypothalamus, insulin takes on many roles involved in energy homoeostasis. Therefore, the aim of this study was to examine hypothalamic insulin expression during the initial phase of the metabolic response to fasting. Hypothalamic insulin content was assessed by both radioimmunoassay and Western blot. The relative expression of insulin mRNA was examined by qPCR. Immunofluorescence and immunohistochemistry were used to determine the distribution of insulin immunopositivity in the hypothalamus. After 6-h fasting, both glucose and insulin levels were decreased in serum but not in the cerebrospinal fluid. Our study showed for the first time that, while the concentration of circulating glucose and insulin decreased, both insulin mRNA expression and insulin content in the hypothalamic parenchyma were increased after short-term fasting. Increased insulin immunopositivity was detected specifically in the neurons of the hypothalamic periventricular nucleus and in the ependymal cells of fasting animals. These novel findings point to the complexity of mechanisms regulating insulin expression in the CNS in general and in the hypothalamus in particular.
T2  - European Journal of Neuroscience
T1  - Short-term fasting promotes insulin expression in rat hypothalamus
IS  - 1
VL  - 46
DO  - 10.1111/ejn.13607
SP  - 1730
EP  - 1737
ER  - 

@article{
author = "Dakić, Tamara B. and Jevđović, Tanja V. and Perić, Mina I. and Bjelobaba, Ivana and Markelić, Milica B. and Milutinović, Bojana S. and Lakić, Iva V. and Jasnić, Nebojša I. and Đorđević, Jelena D. and Vujović, Predrag Z.",
year = "2017",
abstract = "In the hypothalamus, insulin takes on many roles involved in energy homoeostasis. Therefore, the aim of this study was to examine hypothalamic insulin expression during the initial phase of the metabolic response to fasting. Hypothalamic insulin content was assessed by both radioimmunoassay and Western blot. The relative expression of insulin mRNA was examined by qPCR. Immunofluorescence and immunohistochemistry were used to determine the distribution of insulin immunopositivity in the hypothalamus. After 6-h fasting, both glucose and insulin levels were decreased in serum but not in the cerebrospinal fluid. Our study showed for the first time that, while the concentration of circulating glucose and insulin decreased, both insulin mRNA expression and insulin content in the hypothalamic parenchyma were increased after short-term fasting. Increased insulin immunopositivity was detected specifically in the neurons of the hypothalamic periventricular nucleus and in the ependymal cells of fasting animals. These novel findings point to the complexity of mechanisms regulating insulin expression in the CNS in general and in the hypothalamus in particular.",
journal = "European Journal of Neuroscience",
title = "Short-term fasting promotes insulin expression in rat hypothalamus",
number = "1",
volume = "46",
doi = "10.1111/ejn.13607",
pages = "1730-1737"
}

Dakić, T. B., Jevđović, T. V., Perić, M. I., Bjelobaba, I., Markelić, M. B., Milutinović, B. S., Lakić, I. V., Jasnić, N. I., Đorđević, J. D.,& Vujović, P. Z.. (2017). Short-term fasting promotes insulin expression in rat hypothalamus. in European Journal of Neuroscience, 46(1), 1730-1737.
https://doi.org/10.1111/ejn.13607

Dakić TB, Jevđović TV, Perić MI, Bjelobaba I, Markelić MB, Milutinović BS, Lakić IV, Jasnić NI, Đorđević JD, Vujović PZ. Short-term fasting promotes insulin expression in rat hypothalamus. in European Journal of Neuroscience. 2017;46(1):1730-1737.
doi:10.1111/ejn.13607 .

Dakić, Tamara B., Jevđović, Tanja V., Perić, Mina I., Bjelobaba, Ivana, Markelić, Milica B., Milutinović, Bojana S., Lakić, Iva V., Jasnić, Nebojša I., Đorđević, Jelena D., Vujović, Predrag Z., "Short-term fasting promotes insulin expression in rat hypothalamus" in European Journal of Neuroscience, 46, no. 1 (2017):1730-1737,
https://doi.org/10.1111/ejn.13607 . .